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Understanding gastrointestinal anxiety in inflammatory bowel disease

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Created On: 21/09/2026

Gastrointestinal-specific anxiety in IBD

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Key take away

Gastrointestinal-specific anxiety in inflammatory bowel disease is driven primarily by systemic psychological distress rather than local inflammatory activity or tryptophan metabolite levels.

Background

Persistent abdominal symptoms can occur in people with inflammatory bowel disease (IBD) even when objective intestinal inflammation is absent, often presenting as irritable bowel syndrome (IBS)-like symptoms. Gastrointestinal-specific anxiety (GSA), a characteristic feature of disorders of gut-brain interaction, may contribute to these symptoms and could be clinically relevant in IBD sufferers. This study investigated whether GSA is linked with psychological symptoms, IBD disease activity, serotonergic genetic variants, and circulating tryptophan metabolites.

Method

This cross-sectional study included 308 individuals suffering from IBD (mean age, 42.4 ± 19.4 years; 183 women and 125 men) across different states of disease activity. Two additional subsamples were evaluated for biological associations:

Genetic analysis: 83 patients (mean age, 41.2 ± 15.9 years; 37 women and 46 men) were assessed for associations between GSA and single-nucleotide polymorphisms in genes involved in serotonin signaling.
Metabolite analysis: 70 patients (mean age, 42.1 ± 16.1 years; 32 women and 38 men) were evaluated for links between GSA and serum tryptophan metabolites.

Associations between GSA and psychological variables, disease activity, inflammatory biomarkers, serotonergic polymorphisms, and tryptophan metabolites were examined.

Result

Psychological symptoms illustrated significant associations with GSA:

Anxiety: β = .393; p < .001
Depression: β = .284; p < .001

Anxiety was the strongest predictor of GSA, illustrating a greater contribution than disease activity. IBD disease activity was also linked with GSA (β = .171; p = .002). However, inflammatory biomarkers were not considerably related to GSA, suggesting that GSA may not directly reflect objective inflammatory burden.

Genetic analyses identified associations between GSA and certain serotonergic variants. After accounting for multiple testing, none of the identified associations remained statistically significant, suggesting that the genetic findings must be interpreted cautiously. Similarly, serum tryptophan metabolites exhibited no vital links with GSA.

Conclusion

GSA appears to represent a clinically relevant dimension of gut-brain interaction in IBD and is more strongly related to psychological symptoms—particularly anxiety—than to disease activity. The absence of significant associations with inflammatory biomarkers and tryptophan metabolites further suggests that GSA may not simply reflect intestinal inflammation.

Routine assessment of GSA alongside anxiety and depressive symptoms could assist identify gut-brain interaction disturbances and support more individualized care of IBD sufferers, particularly those experiencing persistent IBS-like gastrointestinal symptoms.